The present invention relates to a system and method for electrical stimulation of the inner ear. More particularly, the present invention relates to an implantable device for electrical stimulation of the 8.sup.th nerve. Even more particularly, the present invention relates to an implantable device for electrical stimulation of the 8.sup.th nerve to produce the sensation of hearing.
It is well known that brain and nerve impulses are electrical in nature. It is also known that electrical stimuli applied to receptor centers such as the nerves cause a reaction dependent on the electrical characteristics of the stimuli. Many devices utilize these characteristics to compensate for defective performance of sensory organs of the body.
In normal hearing, the hair cells are a critical link in the hearing chain. They serve two functions in association with the brain: (1) they establish a background nerve activity that is perceived as silence ("active silence" as described below); and (2) when sound enters the ear, they generate a potential that varies and modulates this background nerve activity in response to the sound. The resulting nerve activity is a constant plus the derivative of the atmospheric pressure. This derivative or rate of change of pressure carries the sound information. Important to the present invention is the recognition that the rate or frequency or density of the resultant nerve activity may be viewed as a carrier modulated by sound.
In the profoundly deaf patient, the principal cause of deafness is the loss of function of the hair cells. In 30% of the deaf, the loss of nerve fibers from the spiral ganglion to the non-functioning hair cells is a contributory cause of deafness. This may be caused due to inactivity of the nerve fibers from the hair cells to the spiral ganglion. Therefore, to restore hearing to a person with a partial or total (profound) loss of hearing, a replacement of these functions is required past the point of loss of function, that is at a higher link to the brain.
In the case of the ear and associated hearing functions, many devices have been designed to electrically stimulate the auditory nerve of the human body, which is known as the 8th cranial nerve. However, these devices operate on principles derived from an inappropriate extrapolation of certain observations made by Beckesy in the 1930's. Beckesy's observations concerned the Basilar membrane, which extends the entire length of the Cochlea. These observations revealed that the Basilar membrane vibrates in response to sound vibrations that enter the ear. It was observed by Beckesy, and confirmed by others, that the sound vibrations caused the membrane to vibrate with a standing wave wherein the maximum amplitude of the standing wave occurred at a location on the membrane dependent on the frequency of the entering sound vibrations. Individual hair cell activity at these locations was also particularly pronounced at the locations of the maximum amplitude of the standing wave. High frequencies result in a maximum amplitude at the entrance to the Cochlea. As the frequency decreases, the location of this maximum amplitude moves toward the extreme end of the Cochlea.
While this mechanical action is true and individual hair cell activity is emphasized at these maximum amplitude locations, others have inappropriately extrapolated these observations to conclude that hearing was effected by the response of the individual nerve fibers along the length of the Cochlea that were frequency dependent. Thus, the theory developed, known as the Place Theory of hearing, that the nerve fibers in the Cochlea conduct different frequencies to the brain dependent on their location in the Cochlea. It is curious that the absolute length of the cochlear duct, which varies from 5 mm in the chicken to over 100 mm in the whale, does not seem to play a very important role in the frequency range of the Cochlea, i.e., the whale has a slightly greater frequency range than a chicken even though the Place Theory of hearing would suggests that, with a Cochlea that is 20 times longer, the whale's frequency range should be 20 times greater than the chicken's.
The Place Theory of hearing requires that the nerves in the Cochlea operate in a manner different from the manner in which all other nerves in the body operate. The present invention is based on a model of hearing that is entirely different than the Place Theory. This invention, in contrast to the Place Theory, is based upon the application of signal processing principles to the function of the nerve fibers of the 8.sup.th nerve terminating in the vestibule and Cochlea, much like the operation of modern communication receivers that use Digital Signal Processing to reduce noise and process information.
The nerves terminating in the Vestibule and/or Cochlea that transfer sound sensation are non-specific and may be fired in sequence or as a sustained background nerve activity by a single pulse which, when modulated, produces the sensation of the sound of the modulation for a given period of time. Accordingly, given the principles guiding the present invention, the nerve fibers in the 8.sup.th nerve operate in a manner identical to those throughout the body. In particular, the signal sent by the nerves is non-specific but the number of nerves firing and the rate of firing conveys information to the brain that the brain translates into sound. The number of nerve fibers firing simultaneously or at such a high repetition rate that it appears simultaneous is a function of the instantaneous sound intensity, variations of this nerve activity is perceived as sound.
The model of hearing upon which the present invention is based recognizes that many nerve fibers of the Cochlea have functions other than the conduction of sound. It is recognized that the very regular and orderly spatial arrangement of the sensory elements in the Cochlea predispose it to work on the basis of spatial principles, however, not in accordance with the Place Theory of hearing. It has been observed that stimulation of many of these fibers does not produce the sensation of sound. The brain utilizes the Cochlea as a mechanism to control the sound pressure variations as a result of the sound vibrations and thereby serve as a means of volume control.
In this mode, some of the outer hair cells of the Cochlea sense the motion of the Basilar membrane, transmit this information to the brain which in turn sends back signals to many of the hair cells in the Cochlea to control the stiffness of the Basilar membrane and thereby control the mechanical impedance at the entrance from the Vestibule to the Cochlea. This then allows for an automatic volume control (in the mechanical domain) and possibly a means of controlling the frequency response to improve intelligibility. Changing the mechanical characteristics of the Basilar membrane changes the mechanical transfer of energy to the hair cells thus effecting sensitivity and frequency response. The Cochlea may also contribute to the process of sound localization.
Audio signals of speech and music are found to have most of their energy concentrated in the lower-frequency ranges. To achieve an improvement in the signal-to-noise ratio, preemphasis (boosting the gain of a signal) of the high frequencies should be observed and a corresponding deemphasis at the detection in the brain. Consistent with this notion, Becksey published in 1960 that patterns of vibration of the Cochlear partition of cadavers for various frequencies showed a preemphasis of the high frequencies in the first 10-mm distance from the stapes. In 1974, Rhode published a graph of the input-output ratio, in decibels, for the Malleus and Basilar membrane (FIG. 21A). The graph shows an increase of 6 dB per octave (or 20 dB per decade) of the frequencies between 200 Hz and 8 kHz. Also FIG. 21B shows that a broad range of frequencies stimulates the hair cells in this area. These observations tend to support the concept of preemphasis. Observations also suggest that the outer hair cells of the Cochlea function to provide information to the brain to control volume, the dynamic range and have an effect on frequency response rather than to transmit the sensation of particular frequencies to the brain.
In addition, it is not generally known that the nerve activity that produces sound consists of the summation of the nerve activity in response to external sound or stimuli modulating a constant background nerve activity. This constant background nerve activity was described by R. Lorente De No in 1976 as follows, "In the absence of peripheral stimulation, the acoustic nuclei are the site of continuous activity maintained by the arrival of nerve impulses spontaneously initiated in the Cochlea. The activity is necessarily accompanied by circulation of impulses in chains of neurons.
Since spontaneous activity in the cochlea and in the acoustic centers is perceived by humans as silence, it must be concluded that the spontaneous activity serves to determine the background states of the various subdivisions of the acoustic nuclei, to which the deviations caused by sound are referred. In other words, what we hear is the result of those deviations from the ground states or baseline signal of the acoustic nuclei, which are caused by external sources of sound." He refers to this background state as "active silence" to which perception of sound is referred.
While others have observed this activity, none has recognized it as a carrier that is the summation of non-specific nerve activity and modulated by external stimuli. The recognition of this principle is an important element of the present invention. This recognition is consistent with the sample data-theorem developed by Hartley of Bell Labs and Nyquist in 1928 when one considers the "active silence" as a carrier frequency.
It is not necessary that the nerve activity be a sequence of single nerve fiber activity but that the nerve activity is at such a high frequency that it is beyond the range of audible sound, paring or multiples of simultaneous nerve findings may occur. Active silence can be compared to the molecular activity of a gas at a given pressure (silence) and the modulation of this activity by pressure variations due to sound.
The mechanical characteristics of the Basilar membrane at the entrance to the Cochlea (see FIGS. 21A and 21B) are such that the modulation is maximum for high frequencies and reduces at a rate of 6 dB per octave to the lower frequencies. Audio signals of speech and music are found to have most of their energy concentrated in the lower-frequency ranges. The emphasis of the high frequency components of the audio signal is introduced before the nerve activity noise is introduced, to the point where they produce a constant deviation of the background nerve activity as a function of frequency. This equalization, of the low frequency and high frequency portions of the audio spectrum, enables the signal to fully occupy the bandwidth of the neuron communication link. The spectrum of the noise introduced at the nerve summation output occupies the entire bandwidth. The noise-power spectrum at the output summation is emphasized at the higher frequencies. At the summation output of the nerve fibers the inverse function, deemphasis is introduced to the higher-frequency components, which restores the original signal-power distribution. This deemphasis process reduces the high-frequency components of the noise also and so effectively increase the signal-to-noise ratio.
This function of accentuating the high frequencies compensates for an inverse function at the far end of the nerve bundle in the brain. It is similar to accentuating the high frequencies in a FM transmitter and subsequently attenuating high frequencies at the receiver. The result is, with the Basilar membrane compensation for the brain "receiver" functions, an improved signal-to-noise ratio. A secondary characteristic of the Cochlea is that all frequencies do in fact stimulate nerve fibers near the Vestibule with preemphasis. High frequencies dominate the entrance and low frequencies dominate the other end. However, the sensing of a frequency is not related to which nerve fibers are stimulated but rather to the change in overall nerve fiber activity when looking at the summation of all nerve fiber activity (see FIG. 20)
The foregoing function of the Cochlea might be compared to a woofer, mid-range and tweeter speaker system. When the sounds arrive at the ear, an individual hears the summation of the activity of each of the speakers. Similarly, the brain receives signals that constitute the summation of the activity and signals sent by the hair cells and the associated nerve activity. Importantly, however, the nerve activity associated with each stimulated hair cell makes a contribution to the summated nerve activity entirely independent of the contribution made by the nerve activity of other stimulated hair cells but is effected by other nerve activity. Thus, oftentimes, when observed in isolation, the nerve activity seemed to be frequency selective. However, when looked at closer in light of the recognition of the spontaneous or background activity of the hair cells as a carrier frequency for sound stimuli received, the recognition of the present invention that the modulation of background or spontaneous nerve activity is what is "heard", not the nerve activity associated with individual hair cells, becomes apparent.
While it is true that different frequencies may increase activity of nerve fibers in different areas of the Cochlea, this does not effect the transmission of sound. The summed change in nerve activity from the Vestibule and the Cochlea is heard as sound, not which nerve fiber is activated at any time or when a given frequency is heard. This concept was first suggested by Rinne in 1865 but he had no formal theory to put forward. In 1880 Rutherford provided a plausible explanation, the TELEPHONE THEORY. However at that time little was known of nerve fiber characteristics and it would be almost 50 years before Hartley's and Nyquist's SAMPLE DATA THEOREM.
The physiological characteristics of the 8.sup.th auditory nerve are likewise important in designing any system based on the theory of hearing adopted above. In particular, five characteristics play an important role in the design of any such system: strength-duration, streaming, latency, recovery, and fatigue. The strength-duration characteristics of the human nerve fibers are graphically represented by the strength-duration curve shown in FIG. 1A. The strength duration curve expresses the relation between least strength of an applied current (stimulus) to the nerve fiber and the least time during which the current (stimulus) must flow to reach a threshold for excitation. Expressed another way, the strength-duration curve is a plot of the threshold intensity just capable of exciting an axon and its relationship to the duration of the stimulus current. Indeed, nerve fibers will not excite in response to current densities below a minimum. The strength-duration curve is further described in Medical Physiology and Biophysics, Ruch and Fulton, 18th Edition, W. B. Saunders & Co. Ruch and Fulton model this nerve behavior after a single resistance capacitance circuit. Strength duration combined with a gradient electric field determines the range of pulse length for a stimulus pulse to cause "streaming."
Streaming is the sequential firing of nerve fibers within a group of nerve fibers or ganglia that have been stimulated by a single-pulse stimulus. Upon stimulation by a single-pulse stimulus such as a single square wave through action of a gradient electrical field impinging on a group of nerve fibers or ganglia, the individual nerve fibers within the group will each receive a stimulus decreasing in intensity as the individual nerve fibers within the group increase in distance from the source electrode. This phenomenon is shown in FIG. 1B. The firing rate of the individual nerve fiber will correspond to that shown in the strength-duration curve of FIG. 1A. Thus, when the individual nerve fibers within a stimulated nerve group commence firing, those closer to the origin of the gradient field will fire at a greater rate while those farther away will fire at a slower rate.
Thus, the nerve group will transmit a series of signals, i.e., a stream of nerve activity, over time. In particular, this "streaming" is characterized in that some nerves in the group will fire in succession, which successive firings occurring at a slower rate than the previous firing.
Streaming occurs during the latter portion of a single nerve pulse stimulus. The length of streaming of a group of nerve fibers is limited by the delay of the start of streaming at the beginning of the pulse (no sooner than 0.1 milliseconds according to the strength-duration curve of FIG. 1A) and the time remaining to the end of the stimulus pulse. This behavior is shown at the top portion of the graph of FIG. 1A by the line labeled as the "Nerve Firing Rate." The latency period is the delay between the start of the stimulus pulse and the firing of a nerve fiber.
Reference to FIG. 1A shows that the latency time For each nerve fiber is different as defined by the strength-duration curve and the gradient field. In practice it is desirable to have the starting of streaming to be delayed by more than 0.2 ms. As the latency time is shortened by increasing the stimulus amplitude, the compensation component necessary to keep the differential latency times constant during streaming requires increases the stimulus to an excessive amplitude for a system with a long streaming time, gas in the 4 channel system). The minimum latency period also determines the overlay time for adjacent channels i.e., the time in which the adjacent or other nerve fibers must be stimulated to continue the transmission of the total signal once the original nerve fiber channel enters the recovery stage.
Moreover, the 8.sup.th nerve individual fibers are not capable of indefinitely transmitting stimuli. After receiving and transmitting a stimulus, the nerve must go through a recovery period. Absent this, the nerve will fatigue and will cease transmitting. The recovery characteristics of the nerve limit the repetition rate of individual channel stimulation. Lastly nerves are damaged by prolonged stimulus with an average DC component. All such stimuli must be made in an AC fashion.
When an electrical field impinges on the auditory sensory branch of the 8.sup.th nerve including the brain stem or the spiral ganglion, the angle of arrival produces a gradient field across the nerve group that can causes the nerves to fire in sequence. This is illustrated in FIG. 1C, which indicates how the strength of an electric field decreases across a group of nerve fibers, between a cathode and an anode. Because of this decreasing strength electric field, the nerve fibers fire in sequence. In addition, because of the combination of the electric field and the strength-duration characteristics of the nerve fibers, as the distance from the cathode increase, the time between successive nerve firings also increases. In contrast, with the arrangement shown in FIG. 1D, all of the nerve fibers are subject to substantially the same electric potential and will thus fire substantially simultaneously.
If the stimulus amplitude is small, so as not to produce a high enough carrier frequency to be above the range of hearing the streaming frequency can be heard. Its frequency is a function of the stimulus place on the strength-duration curve in relation to the nerve fibers stimulated and the curve's slope. This varies with time and amplitude of the stimulus. As mentioned above, the signal sent by the nerves is non-specific but the number of nerves firing and the rate of firing conveys information to the brain that the brain translates into sound. For example, as the amplitude is increased, the rate of sequential nerve fiber firing increases. If the angle of a stimulus is near perpendicular a high rate of sequential firing will occur as the individual nerve fibers of a channel receive close to the same stimulation. If the angle is small the sequential firing is at a lower frequency as the difference of stimulation across the individual nerve fibers stimulated will have a greater range.
Known devices which are designed to aid the profoundly deaf by electrical stimulation of the 8.sup.th nerve but on principles guided by the Place Theory, however, function primarily because of this angle and stimulus dependency, but with results that are not predictable, repeatable or optimized. In U.S. Pat. No. 3,449,768, issued to James Doyle, the system was not designed based on principles of the Place Theory of hearing but was designed to produce a carrier of nerve activity based on multiple channels stimulated in sequence at a rate sufficiently high to result in a carrier of nerve activity suitable for modulation with sound information. That patent discloses a device for applying electrical stimuli to the 8.sup.th cranial nerve and includes an electrode system for placement in the vicinity of the auditory nerve, means for feeding pulses to a plurality of transmission channels and a modulator which modulates a time-amplitude integral of each of the pulses.
This system was limited because, for example, of the number of channels required and the recovery time allowed for each channel was too short to allow for prolonged stimulus without causing nerve fatigue. No consideration was given to the latency characteristics of nerve fibers (the delay between the start of the stimulus pulse and the firing of a nerve fiber). Moreover, the earlier Doyle system failed to allow for compensation in the stimulus strength to maintain a constant nerve firing rate and overcome the inherent slowing due to streaming, as described above. Lastly, the earlier Doyle patent did not recognize or teach that the carrier frequency (the frequency or density of the background nerve activity) is independent of the rate at which the individual channels are being fired and the number of the individual channels. These limitations or failures resulted in a system with low sound fidelity, a signal to noise ratio that is lower than can be achieved otherwise, and a constant hum or tone perceived by the patient.